Cells are constantly talking with each other, mostly with the help of cell surface receptors and ligands. This includes information on the amount of 'self-digestion' to perform. Higher self-digestion, or autophagy, leads to faster protein turnover and has been implicated in many age-related diseases, esp. those with an autoimmune component. Could we understand the mechanism controlling levels of autophagy and modulate it to affect disease outcomes?
Anu Chaudhary and her colleagues display an elegant way to screen human genetic variation underlying any observable phenomena. By focusing on response to rapamycin, a drug that induces autophagy, they were able to isolate variations that enhance cellular self-digestion. They use this to characterize cell surface receptors that can vary autophagy levels, and use this knowledge to develop means that could deter auto-antibody production. To learn more about the exciting and relevant finding, please listen to Anu.
For further information, please refer:
Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.
Chaudhary et al., Current Biology, 2016.
Anu Chaudhary and her colleagues display an elegant way to screen human genetic variation underlying any observable phenomena. By focusing on response to rapamycin, a drug that induces autophagy, they were able to isolate variations that enhance cellular self-digestion. They use this to characterize cell surface receptors that can vary autophagy levels, and use this knowledge to develop means that could deter auto-antibody production. To learn more about the exciting and relevant finding, please listen to Anu.
For further information, please refer:
Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.
Chaudhary et al., Current Biology, 2016.
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